Experimental fat embolism induces urine 2,3-dinor-6-ketoprostaglandin F(1α) and 11-dehydrothromboxane B2 excretion in pigs

Markku Rautanen, Eero Gullichsen, Asko Riutta, Kari Kuttila, Istvan Mucha, Olavi Nelimarkka, Juha Niinikoski

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Objective: To evaluate the in vivo production of prostacyclin and thromboxane A2 during the initial phase of experimental fat embolism as assessed, respectively, by determinations of urine 2,3-dinor-6- ketoprostaglandin F(1α) and 11-dehydrothromboxane B2 excretion. Design: Randomized, controlled trial. Setting: Animal laboratory. Subjects: Twenty seven domestic pigs, weighing 24 to 31 kg. Interventions: All pigs were anesthetized and mechanically ventilated during the experiment. Eighteen pigs were subjected to an intracaval infusion of 10% allogeneic bone marrow suspension at e dose of 100 mg/kg over 5 mins. Nine pigs received only bone marrow suspension (fat embolism group). Nine pigs were given an intravenous bolus of aspirin (300 mg) 1 hr before the bone marrow suspension infusion. After the induction of fat embolism, intravenous aspirin was administered at a dose of 150 mg/hr for 2 hrs (aspirin-treated group). Nine pigs were infused with saline (control group). Measurements and Main Results: in the fat embolism group, cardiac index decreased within 30 mins, while mean arterial pressure remained unchanged. Central venous pressure and pulmonary artery occlusion pressure remained relatively stable over time in the animals with fat embolism. Mean pulmonary arterial pressure and pulmonary vascular resistance increased immediately after the bone marrow suspension infusion from 23 ± 0.8 (SEM) to 34 ± 1.3 mm Hg and from 305 ± 28 to 585 ± 45 dyne · sec/cm5, respectively; these variables remained increased throughout the study period. Simultaneously, pulmonary shunt in the fat embolism group increased persistently from the baseline of 12.3 ± 2.8%, and reached its maximum of 26.1 ± 4.8% at the end of the experiment. Instant and gradual decreases in PaO2 (from 95 ± 4 to 67 ± 5 torr [12.6 ± 0.5 to 8.9 ± 0.7 kPa]), hemoglobin oxygen saturation (from 97.2 ± 0.4 to 91.8 ± 1.8%), and oxygen delivery (from 16.3 ± 1.0 to 12.6 ± 0.4 mL min/kg) were observed in the fat embolism group. In the bone marrow suspension-infused animals, urine 2,3-dinor-6-ketoprostaglandin F(1α) excretion increased transiently from 451 63 up to 1466 ± 499 pg/μmol creatinine, while urine 11-dehydrothromboxane B2 excretion increased transiently from 385 36 up to 2307 ± 685 pg/μmol creatinine. In the aspirin-treated animals, urinary excretion of these prostanoid metabolites was reduced by 81% and 88%, respectively. The changes in mean pulmonary arterial pressure and PaO2 were ameliorated, and the alterations in pulmonary shunt and SaO2 were abolished in the animals with aspirin treatment. Conclusions: Pulmonary hypertension, increased pulmonary vascular tone, and increased pulmonary shunt are hallmarks of the present fat embolism model. These hemodynamic responses may, at least partly, be related to the changed balance between prostacyclin and thromboxane A2 production.

Original languageEnglish
Pages (from-to)1215-1221
Number of pages7
JournalCritical care medicine
Issue number7
Publication statusPublished - Jul 1 1997


  • 2,3- dinor-8-ketoprostaglandin F(1α) 11-dehydrothromboxane B
  • Fat embolism
  • Hypoxemia
  • Lung injury
  • Prostacyclin
  • Prostaglandin metabolites
  • Pulmonary hemodynamics
  • Thromboxane A
  • Vasoconstriction

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

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